SHOCK AND MULTISYSTEM DISORDERS
1.5 NCM 118: Critical Care Nursing
Dr. Socorro S. Gasco, RN, MN, DM • January 14, 2022
SHOCK
• It is a life-threatening condition (precisely this is
under critical care)
• Potentially lethal, debilitating, and costly (people
would really spend so much in hospitalization, they
are not sure if they will survive)
• Defined as failure of the circulatory system to
maintain adequate perfusion of vital organs (such us
the lungs, liver, heart, kidney, brain)
CLASSIFICATION OF SHOCK
1. HYPOVOLEMIC SHOCK
⎯ due to inadequate circulating blood
volume resulting from hemorrhage with
actual blood loss (shock due to low blood
volume), burns of massive shifts of fluids
due to movement of plasma proteins into
interstitial spaces, and fluid shifts or
dehydration, with or without loss of fluid
volume
⎯ develops when the intravascular volume
decreases (due to burns, dehydration) to
the point where compensatory
mechanisms are unable to maintain
organ and tissue perfusion.
2. CARDIOGENIC SHOCK
⎯ due to inadequate pumping action of the
heart (heart attack, MI, CAD). The heart
muscle can be diseased as a result of
primary cardiac muscle dysfunction or
mechanical obstruction of blood flow
caused by myocardial infarction (MI),
valvular insufficiency (due to rheumatic
heart disease) caused by disease or
trauma (vehicular accident, gunshot
wounds, or penetrating wounds), cardiac
dysrhythmias (heart blocks), or an
obstructive condition such as cardiac
tamponade (there is water in the
pericardial area) or pulmonary embolus.
The clinical definition of cardiogenic
shock is decreased cardiac output and
evidence of tissue hypoxia in the
presence of adequate intravascular
volume. There is 60 ml of blood per beat
x 72 beats per minute. Below 60 ml, the
tissues can no longer be perfused.
HEMODYNAMIC CRITERIA FOR
CARDIOGENIC SHOCK
a. Sustained hypotension (systolic
blood pressure <90mmHg for at
least 30 min)
b. Reduced cardiac index (<2.2
L/min/m2)
OTHER MANIFESTATIONS OF TISSUE
HYPOPERFUSION
• oliguria (<30ml/hr)
Normal urine is 1 ml/minute. There
should be 60 ml of urine per hour.
• cool extremities
Due to lack of blood supply
• altered mentation
altered state of consciousness
BAUTISTA, BALMES, BELARMINO, BARCELON
o Cardiogenic shock after an MI usually occurs
when 40% or more of the myocardium has been
damaged.
o The term OBSTRUCTIVE SHOCK is sometimes used
to include conditions that lead to a sudden
obstruction of blood flow e.g., cardiac tamponade,
tension pneumothorax, pulmonary embolism,
thrombus, embolus
3. DISTRIBUTIVE SHOCK/ VASOGENIC
SHOCK
⎯ due to changes in blood vessel tone that
increase the vascular space without an
increase in the circulating blood volume.
3 TYPES OF DISTRIBUTIVE SHOCK
a. Anaphylactic shock
⎯ severe hypersensitivity reaction
resulting in massive systemic
vasodilation (sensitivity due to drugs,
bee sting, insect bites, allergy to
foods).
b. Neurogenic shock
⎯ interference with nervous system
control of the blood vessels, can
occur with conditions such as spinal
cord injury (especially cervical spine
injury, severe spinal injury in
vehicular accident or fall), spinal
anesthesia, or severe vasovagal
reactions caused by pain or psychic
trauma.
c. Septic Shock
⎯ caused by the release of vasoactive
substances. Current theories suggest
there is a cascade of interactions
between immune cells that happens
rapidly that leads to microcirculatory
alterations.
ETIOLOGY
1. HYPOVOLEMIC SHOCK
a. Hemorrhage
⎯ loss of blood (emergency blood
transfusion is needed)
⎯ blood volume deficit of 15% to 25%,
or about 500 to 1500 ml in an adult
⎯ wounds of the chest, abdomen
(abdominal aorta), and thighs can
lead to hemorrhagic shock.
b. Burns
⎯ large partial-thickness or full
thickness burns
⎯ caused primarily by a shift of plasma
from the vascular space into the
interstitial space.
⎯ client may have cardiac dysfunction
that is due to the presence of
myocardial depressant factor (MDF)
⎯ Fluid shifts similar to those in burns
include nephrotic syndrome (people
with nephrotic syndrome have
generalized edema known as
anasarca), severe crush injuries
(vehicular accident), starvation,
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 SHOCK AND MULTISYSTEM DISORDERS
1.5 NCM 118: Critical Care Nursing
Dr. Socorro S. Gasco, RN, MN, DM • January 14, 2022
surgery and conditions causing
plasma fluids to accumulate in the
abdominal cavity (e.g. cirrhosis of
the liver, pancreatitis, bowel
obstruction)
c. Dehydration
⎯ reduced oral fluid intake from
significant fluid losses (e.g. rigorous
exercise causing fluid loss from
sweating and insensible fluid loss
through the respiratory tract and in
hot environment)
⎯ excessive urine output (Diabetes
insipidus) or prolonged vomiting or
diarrhea, leading to dehydration-
induced hypovolemic shock
(Dysentery, Cholera – dies due to
dehydration)
⎯ an inability to obtain fluids,
inadequate maintenance of chronic
conditions (e.g. increased blood
glucose levels with diabetes)
⎯ Inadequate monitoring of
therapeutic regimens (e.g. diuretic-
induced dehydration)
2. CARDIOGENIC SHOCK
a. Myocardial infarction
⎯ impaired heart muscle action is most
often caused by MI (obstruction in
the coronary arteries, so the muscles
in the heart are not perfused with
blood. Remaining muscles die)
⎯ the area of dead or dying tissue that
occurs with infarction impairs
contractility (due to necrosis) of the
myocardium and cardiac output (15-
25%) decreases
⎯ impaired myocardial contractility
(heart cannot contract that is why
there is 15-25% blood deficit) may
also occur with blunt cardiac trauma
(vehicular accident, gunshot wound),
cardiomyopathy, and heart failure
b. Obstructive Conditions
• Large Pulmonary Embolism
⎯ an embolus is usually the result
of a blood clot that breaks loose
in a person with deep vein
thrombosis (DVT)
A thrombus that travels becomes
an embolus
⎯ this embolus travels through the
venous system to the right side
of the heart and into the
pulmonary artery
• Pericardial Tamponade
⎯ accumulation of blood or fluid in
the pericardial space (outer
layer of the heart) that
compresses the myocardium
and interferes with the ability of
the myocardium to expand or
contract.
• A Tension Pneumothorax
⎯ significant amount of air
in the pleural space that
BAUTISTA, BALMES, BELARMINO, BARCELON
compresses the heart and great
vessels, thus interfering with
venous return to the heart.
When you want to belch, the air
compresses the heart, then
chest pain occurs.
OTHER CAUSES OF CARDIOGENIC SHOCK
1. Cardiac Valvular insufficiency from
trauma or disease (in rheumatic heart
disease wherein the valve flaps are
involved)
2. Myocardial aneurysms (aneurysm in the
coronary arteries)
3. Rupture of a valvular papillary muscle
(rupture of the valves such as tricuspid
valve, mitral valve, pulmonic valve, aortic
valve. Usually mitral is involved)
4. Ventricular rupture (if there is left
ventricular hypertrophy. Left ventricle
dilates due to prolonged high blood
pressure. Excessive dilation or
hypertrophy would cause rupture -
ventricular rupture)
5. Aortic stenosis (the aortic valve leading
to the aorta, blood from the left ventricle
going to the aorta. Sometimes in aortic
valve, there is stenosis, this may be due
to inflammatory conditions such as
rheumatic fever, or it could be
congenital)
6. Mitral regurgitation (mitral valve
connecting the left ventricle and left atria
is defective due to rheumatic heart
disease, rheumatic fever, or congenital.
Blood in the left atrium cannot flow. Not
all of the blood will enter the left
ventricle, some will come back to the left
atrium because the mitral valve cannot
close. Normally, when the heart
contracts, the valves close)
7. Cardiac dysrhythmias (heart block. There
is lack of connection between the SA
node and AV node because of the
problem in electrical activity, there is no
rhythm)
8. Infectious and inflammatory processes
such as myocarditis and endocarditis
9. Pulmonary hypertension (due to left
ventricular hypertrophy, patent ductus
arteriosus, right-sided heart failure)
10. Toxic drugs
3. DISTRIBUTIVE (VASOGENIC) SHOCK
⎯ size of the vascular space
increases dramatically because of massive
vasodilation
⎯ result is maldistribution of the blood
because of decreased blood pressure
(BP)/hypotension and lack of blood
returning to the heart
⎯ it is often referred to as “relative”
hypovolemia
⎯ volume of blood remains constant, but the
blood has pooled because of increased
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 SHOCK AND MULTISYSTEM DISORDERS
1.5 NCM 118: Critical Care Nursing
Dr. Socorro S. Gasco, RN, MN, DM • January 14, 2022

capacity of the vascular system of hypoperfusion

- Septic shock is defined as sepsis with
a. Acute Allergic Reaction persistent hypotension despite fluid
(Anaphylactic Shock) resuscitation and resulting tissue
⎯ common sensitizing agents are hypoperfusion.
Penicillin, Penicillin derivatives, bee - Bacteremia is the presence of viable
stings, chemotherapy, latex, bacteria in the blood. Bacteremia may be
chocolate, strawberries, peanuts, primary (without an identifiable focus of
snake venom, iodine-based infection)
contrast for X-ray studies, seafood
and nonsteroidal anti- Pathophysiology
inflammatory drugs (NSAIDS), - Shock occurs when there is not adequate
food, vaccination circulating volume to maintain aerobic
⎯ re-exposure to the foreign metabolism in the cells.
substance results in the offending - Adequate circulating volume is dependent on
antigen binding to previously three interrelated components of the
synthesized immunoglobulins (e.g. cardiovascular system:
IgE) on the mast cell ⮚ The heart
⎯ this binding causes the release of ⮚ Vascular tone
histamine
⮚ Blood volume
MANIFESTATIONS - If the heart muscle cannot pump effectively,
o Massive vasodilation cardiac output falls.
o Urticaria (hives) - Vascular tone refers to degree of constriction
o Laryngeal edema (cannot by the smooth muscle in the arteriole.
breathe due to edema in the - If one of the three components of circulation
larynx, this leads to death) falls, other parts of the system initiate
o Bronchial constriction compensatory mechanisms. For example,
vasoconstriction and increased cardiac
b. Spinal Cord Injury (Neurogenic output to compensate for decreased volume.
Shock)
⎯ injuries around the T6 level Cardiogenic shock:
⎯ below the level of injury there is - Is failure of the left ventricle to pump
blocking of sympathetic nervous adequate blood volume
stimulation - When cardiac output falls, the body
⎯ the parasympathetic system acts compensates by releasing catecholamines
unopposed (epinephrine and norepinephrine) to increase
⎯ this unopposed stimulation heart rate and systemic vascular resistance to
causes vasodilation, decreased increase venous return.
cardiac output and decreased - The diseased heart cannot maintain its own
tissue perfusion myocardial tissue oxygenation, which results
⎯ neurogenic shock is manifested in a spiral of decreased cardiac output,
by the triad of hypotension, hypotension and further myocardial ischemia
bradycardia, and hypothermia
⎯ after injury, protect the client’s Anaphylactic shock:
spine, maintain the airway and - When a sensitized client comes in contact
breathing (oxygen), provide with an antigen, IgE is stimulated and the
circulatory support (plasma, blood mast cells and basophils release large
transfusion) and provide for amounts of histamine. Histamine leads to
thermoregulation (blanket) vasodilation, bronchial constriction,
c. Infection (Septic Shock) bronchorrhea, pruritus, laryngeal edema and
⎯ Sepsis is the presence of infection angioedema.
and activation of the inflammatory
cascade (tooth decay, liver Septic shock:
inflammation, inflammation of uterus - About 50% of clients with septic shock have
can cause septic shock) bacteremia, with gram-negative rods and
⎯ Systemic inflammatory response gram-positive organism being the most
syndrome (SIRS) exists in two of the common agents.
following four clinical parameters: - Endotoxins (also called lipopolysaccharides)
o Body temperature are produced by gram-negative organisms.
o Heart rate - Gram-positive cocci also produce exotoxins.
o Respiratory rate - Host resitance and organism virulence are
o Peripheral leukocyte count both factors that determine the body’s
- Sepsis is defined as the presence of SIRS in response. Gram-negative (endotoxins) and
the setting of infection. gram-positive (exotoxins)
- Severe sepsis is defined as sepsis with - Initially, there is an overwhelming
evidence of end-organ dysfunction as a result inflammatory response to the microbes that

BAUTISTA, BALMES, BELARMINO, BARCELON 3

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 SHOCK AND MULTISYSTEM DISORDERS
1.5 NCM 118: Critical Care Nursing
Dr. Socorro S. Gasco, RN, MN, DM • January 14, 2022
is regulated by tumor necrosis factor (TNF),
interferon, and the interleukins.
- Mediators with vasodilatory and endotoxic
properties are released systemically,
including prostaglandins, thromboxane A2
and nitric oxide.
- Results in vasodilation and endothelial
damage, which leads to hypoperfusion and
capillary leakage.
- Cytokines activate the coagulation pathway,
resulting in the capillary microthrombi and
end-organ ischemia.
STAGES OF SHOCK
1. Nonprogressive Stage
- Cardiac output is slightly decreased because
of the loss of actual or relative blood volume
- Body’s compensatory mechanism can
maintain BP within a normal to low-normal
range and can maintain perfusion to the vital
organs.
- During the compensatory phase, the
systemic circulation and microcirculation
work together in a hyperdynamic state.
- This hyperdynamic state leads to an increase
in lactic acid levels.
2. Progressive Stage
- If shock and the compensatory
vasoconstriction persist, the body begins to
decompensate and the systemic circulation
and microcirculation no longer work in
unison.
- As vasoconstriction continues, the supply of
oxygenated blood to the tissues is reduced.
- This results in anaerobic metabolism and
further lactic acidosis.
- Acidosis and the increasing PaCo2 cause the
microcirculation to dilate.
- This dilation causes decreased in venous
return and decreased circulation of
reoxygenated blood.
- Increased vascular capacity, decreased blood
volume, or decreased heart action reduces
the mean arterial pressure (MAP)
- Pressure gradient for the venous return of
blood decreases.
- This also contributes to venous pooling of
blood, decreased venous return to the heart,
decreased cardiac output. Kon low an
cardiac output, low blood an nakadto ha
systemic circulation , there is low tissue
perfusion leading to tissue death or necrosis.
- The result is a low central venous pressure
(CVP) and inadequate venous return to the
right side of the heart, with further decrease
in cardiac output.
- This resultant decrease in circulating volume
and capillary flow does not allow adequate
perfusion and oxygenation of vital organs.
- With the prolonged decrease in capillary
blood flow, the tissues become hypoxic.
3. Irreversible Stage
- The irreversible stage of shock occurs if the
BAUTISTA, BALMES, BELARMINO, BARCELON
cycle of inadequate tissue perfusion is not
interrupted.
- The shock becomes progressively more
severe, even though the initial cause of the
shock is not itself becoming more severe.
Cellular ischemia and necrosis lead to organ
failure and death. Cellular ischemia kay
waray na blood supply, lead to cellular
necrosis then eventually cellular death.
SYSTEMIC EFFECTS OF SHOCK
1. Respiratory system
- Circulatory deprivation results in tissue
hypoxia and anoxia.
- Respiratory failure continues to be a major
cause of death in shock.
- Aspiration and loss of neurologic control of
breathing.
2. Acid-Base Balance
- Oxygen and nutrients are essential to life
because they synthesize adenosine
triphosphate (ATP). ATP is the ultimate
source of energy for life processes. When
oxygen is not present, ATP is produced
through anaerobic metabolism.
- Anaerobic metabolism produces anaerobic
metabolites, such as lactic acid (which causes
intracellular acidity with consequent cellular
damage) and substrates of the adenylic acid
system (which depress the heart)
- In response to the chemoreceptors sensing
decreased pH, the rate and depth of
respirations are increased to “blow-off”
(exhale ) Co2 to compensate for the
metabolic acidosis. This results to respiratory
alkalosis.
- Because lactic acid is not exhaled, it
accumulates in tissue fluids, which become
increasingly acidic. Metabolic acidosis is
eventually produced.
- Acidotic reaction resulting from metabolic
acidosis ultimately kills the cells. The buildup
of lactic acid causes such a severe local
acidosis that cellular enzymes are inactivated.
Cells soon die.
3. Respiratory Alkalosis or Respiratory Acidosis
- Perfusion and oxygen delivery to the tissue
decrease, cellular energy production
decreases. To compensate, cells increase
anaerobic metabolism, which results in the
build-up of lactic acid in the cell.
- As the pH of the cells decrease, lysosomes
within the cell explode, releasing the
powerful, destructive enzymes.
- The enzymes destroy the cellular membrane
and digest the cell contents.
4. Lysosomal Enzymes
- Lysosomal enzymes are released from dead
cells undergoing autolysis.
- During shock, however, the accompanying
metabolic acidosis accelerates the activation
of lysosomal hydrolases within the cells and
their release into the circulation markedly
exacerbate the tissue injury that occurs
during shock.
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1.5 NCM 118: Critical Care Nursing
Dr. Socorro S. Gasco, RN, MN, DM • January 14, 2022
- The release of active lysosomal proteases
and other enzymes from damaged tissue into
the bloodstream and their action on
extracellular and intracellular structures
probably contribute to the progression of
injury from cell to cell.
5. Myocardial Deterioration
- MDF, a polypeptide with vasoactive
properties, released in response to ischemia
of the gastrointestinal (GI) tract. It causes
significant reduction in cardiac output.
- Myocardial zonal lesions, which appear in the
myocardium after ischemia or infarction.
- Cells in these areas do not fully repolarize and
thus interfere with the usual efficient
electrical conduction in the heart, which
results in impaired contraction and possibly
cardiac failure.
6. Disseminated Intravascular Coagulation
- Anaerobic metabolism increases the
production of lactic acid.
- The slow-moving acidic blood
hypercoagulable.
- Hemolysis (destruction of red blood cells with
the liberation of hemoglobin) accompanies
trauma, especially when massive crushing
injury occurs.
- DIC is associated with multiple thrombi or
emboli that are deposited in the
microvascular circulation, with resultant
organ obstruction and increased tissue
ischemia.
- Because of the inappropriate clotting that
occurs with DIC, the body attempts to
reverse the process by breaking down clots.
- This results in bleeding in areas previously
sealed by clots (e.g. venipuncture sites,
vascular leaks in the brain)
- As DIC progresses, clotting factors are
depleted, causing an inability to form normal
clots in the presence of bleeding.
7. Vasoconstriction
- Increased levels of CO2 dilate arterioles
located in active tissues and constrict those
in nonactive tissues.
- Because of the heart’s increased activity,
excessive CO2 is produced in the
myocardium.
- Increased concentration of CO2 directly
dilates the coronary arteries leading to the
myocardium, which allows myocardium to
receive more arterial blood.
- Co2 is also a powerful stimulant of the
vasoconstrictor center in the sympathetic
nervous system.
8. Vasoactive Substances
- The influence they exert may be altered by
factors such as pH, the specific tissue (e.g.
heart, lung), the presence of drugs or other
substances, serum electrolyte levels and
sensitivity of the end organ.
9. Catecholamines
- Catecholamines, such as epinephrine and
norepinephrine, are present early in shock
and are related to the fight-or-flight
response.
BAUTISTA, BALMES, BELARMINO, BARCELON
- Their general effects are to increase blood
flow to the brain, heart, and striated
(skeletal) muscle and to decrease blood flow
to the skin, kidneys and splanchnic bed.
- Sustained vasoconstriction to stagnant
hypoxia and cellular death.
10. Vasoactive Polypeptides
a. Histamine- causes vasodilation,
increased capillary permeability,
bronchoconstriction, coronary
vasodilation and cutaneous reactions
(flares, wheals)
b. Bradykinin- a kinin peptide, bradykinin
produces vasodilation, increased
capillary permeability, smooth muscle
relaxation, pain, and infiltration of an
area with leukocytes.
c. Angiotensin- results from the action of
renal renin on angiotensinogen which
causes vasoconstriction and increased
vascular resistance.
is d. MDF – is a vasoactive polypeptide that
contributes to cardiac failure in clients in
shock by depressing cardiac muscle
contraction.
11. General adaptation Syndrome Response
- Neuroendocrine responses during shock are
defensive reactions that occur during the
body’s stage of resistance in the general
Adaptation Syndrome (GAS).
12. Adrenal Response
- The release of epinephrine and
norepinephrine from the adrenal medulla
(which results in increased respiratory and
heart rates , increased BP, increased blood
flow to organs, decreased blood flow to
peripheral tissues).
- Release of mineralocorticoids (which control
fluid and electrolyte balance) and
glucocorticoids (which increase blood glucose
levels and reduce pain) from the adrenal
cortex.
- The main mineralocorticoids-aldosterone
deoxycorticosterone-help increase
intravascular fluid volume by stimulating the
kidneys to retain sodium and water.
- Aldosterone is essential to the conservation
of sodium. Because water is retained in the
body along with sodium, urine excretion is
diminished during shock. This fluid is retained
in the bloodstream to increase blood volume.
Increasing the blood.
13. Pituitary Response
- ADH is produced by the posterior pituitary
gland.
- The osmolality (osmotic concentration) of the
blood increases with dehydration. That
stimulates osmoreceptors in the
hypothalamus to release ADH from the
posterior pituitary gland. ADH is carried via
the blood to the kidneys, where it causes the
body to retain water.
14. Metabolic Response
- These fuels (e.g. amino acids, fatty acids,
glucose) are produced by the breakdown of
food. These substances are then chemically
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1.5 NCM 118: Critical Care Nursing
Dr. Socorro S. Gasco, RN, MN, DM • January 14, 2022
converted into energy, resulting in the
formation of ATP.
- The glucocorticoids particularly
hydrocortisone, mobilize energy stores.
- Protein catabolism and negative nitrogen
balance occur as part of the metabolic
response because of glucogenesis (resulting
from glucocorticoid action) and salivation.
15. Neurologic response
- With shock, cerebral blood flow and cerebral
metabolism may become insufficient to
maintain normal mental level of
consciousness. Because the brain is totally
dependent on oxygen and glucose and to
fluid imbalances. When the brain becomes
hypoxic, the cerebral vessels dilate to restore
blood flow.
16. Immune System
- All forms of shock severely depress
macrophages, which are located in both the
blood and the tissues. The capacity of
macrophages to remove bacteria is greatly
reduced.
- Alterations in the blood itself are partially due
to tissue hypoxia and impairment of
monitoring activities of the macrophage.
17. Gastrointestinal System
- Under sympathetic stimulation, vagal
stimulation to the GI tract slows or stops,
resulting in ileus with an absence of
peristalsis. A lack of nutrient blood supply to
the intestines increases the risk of tissue
necrosis and sepsis.
- Shock causes serious changes in the function
of the liver, the major organ of detoxification.
The liver suffers from this impaired
circulation and appears to be a source of toxic
materials.
- During shock, the anoxic liver develops
metabolic deficiencies, has an impaired ability
to detoxify, and may release vasoactive
substances.
- In addition, enhanced bacterial invasion of
the liver from the intestines apparently
occurs.
- During shock, pooling of blood occurs in the
viscera. Pooling of blood in the liver and
portal bed may result when masses of
agglutinated (clotted) blood plug numerous
small hepatic vessels, sinusoids, and
intrahepatic radicles of the portal vein and
hepatic artery.
18. Renal System
- Urine production decreases and levels of urea
nitrogen and creatinine increase.
19. Altered Capillary Blood Pressure and Glomerular
Filtration
- Inadequate perfusion of renal capillaries is
believed to be the cause of early prenatal
failure in shock. The afferent and efferent
arterioles constrict, shunting blood away
from the glomeruli. If shock persists, actual
renal shutdown occurs from focal tubular
necrosis.
- Vasoconstriction in the kidneys may continue
for a prolonged time after the systemic BP is
BAUTISTA, BALMES, BELARMINO, BARCELON
restored to normal levels.
20. Renal Ischemia
- During shock, the kidneys, may experience
renal ischemia.
- When injury to the kidneys is extensive and
renal failure ensures, acute tubular necrosis
(ATN) occurs.
CLINICAL MANIFESTATIONS
Systemic Manifestation of Shock:
1. Respiratory System
- Rapid, shallow respirations (tachypnea)
because of decreased tissue perfusion.
- Respiratory rate increase as the oxygen-
carrying capacity of the blood decreases.
These changes may signal development of
hypoxemia and respiratory alkalosis.
2. Cardiovascular System
− Tachycardia. Increased heart rate is the
result of increased sympathetic stimulation.
It is an attempt to maintain adequate cardiac
output and MAP when the blood’s circulating
volume declines.
− The pulse rate may become extremely slow
in the terminal stages of shock.
− Hypotension. The diastolic BP indicates the
resistance (systemic vascular resistance
(SVR) or vasoconstriction) of blood vessels.
3. Neuroendocrine System
− Client feels anxious, nervous, and irritable.
4. Renal System
− Decrease in urinary volume (oliguria)
CLINICAL MANIFESTATIONS OF SPECIFIC TYPES
OF SHOCK
● HYPOVOLEMIC SHOCK
o Sympathetic stimulation increases pulse rate
and respirations and decreases tissue
perfusion to the skin, causing the skin to feel
cool, clammy from diaphoresis, and to appear
pale. Clients may sweat profusely, which
increases insensible fluid loss, leading to
further hypovolemia and temperature
instability. Cyanosis may indicate either
decreased tissue perfusion or decreased
oxygenation.
● CARDIOGENIC SHOCK
o Jugular venous distention
o Increased CVP
o Pulmonary edema – bc of decreased capillary
permeability
o Crackles in the lungs
o Increased pulmonary capillary wedge
pressure (PCWP)
● DISTRIBUTIVE SHOCK
o ANAPHYLACTIC SHOCK
▪ headache
▪ severe anxiety
▪ dizziness
▪ disorientation
▪ loss of consciousness
▪ most common sign: laryngeal edema
and chest tightness
▪ feeling of lump in the throat which is
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1.5 NCM 118: Critical Care Nursing
Dr. Socorro S. Gasco, RN, MN, DM • January 14, 2022

due to laryngeal edema and is tourniquet 9as

followed by hoarseness, coughing, last resort)
dyspnea, and stridor. Diffuse
wheezes and prolonged expiratory
phase ● Reduce
▪ pruritus and urticaria intraabdominal
▪ edema of eyelids, lips, or tongue 9 or
(angioedema) retroperitoneal
bleeding or
o NEROGENIC SHOCK prepare for
▪ Bradycardia and hypotension emergency
▪ Skin temperature takes on the same
surgery.
temperature as the room
(poikilothermia)
▪ Skin is dry to the touch because of
an inability to sweat.
G.I. bleeding
o SEPTIC SHOCK ● Administer
▪ Hypotension lactated
▪ Coagulation disorders Ruptured ringer’s
▪ Multisystem organ dysfunction of Aortic solution or
septic shock due, in part, to a Aneurysm normal saline
dysregulated expression of the
body’s mediators of inflammation.
● Transfuse with
DIAGNOSTICS
1. Complete blood cell count fresh frozen
2. Blood chemistry plasma,
3. Body fluid cultures platelets, or
4. ABG analysis other clotting
− A low PaCO2 along with low pH and factors, if
bicarbonate levels (metabolic acidosis), significant
indicates that hyperventilation is trying to improvement
compensate. ● Does not occur
5. CVP Measurement with crystalloid
− A pulmonary artery or Swan-Ganz Surgery administration.
catheter may also be invested to assist
with assessments of fluid status, cardiac
function, and tissue oxygen consumption
● Use of non-
MEDICAL MANAGEMENT blood plasma
1. correct the causative factor expanders
(albumin,
2. improve oxygenation
hetastarch,
● oxygen can be delivered via nasal dextran) until
cannula, a mask high-flow, a mask, high- blood is
Erosion of the
available,
flow non-rebreathing mask vessel from
Conduct
lesion, tubes
● Endotracheal; intubation or autotransfusion
or other
if appropriate
tracheostomy devices.

SUMMARY OF MANAGEMENT OF

HYPOVOLEMIC SHOCK ● Administer low-

dose
cadiotonics
Etiology Clinical Intervention
(dopamine,
situation
dobutamine)
Blood loss Massive ● Stop external;
trauma bleeding with
direct pressure, ● Administer
with pressure lactated
dressing, ringer’s

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 SHOCK AND MULTISYSTEM DISORDERS
1.5 NCM 118: Critical Care Nursing
Dr. Socorro S. Gasco, RN, MN, DM • January 14, 2022

solution or (eg: diabetic

normal saline ketoacidosis,
Crystalloid heat
loss exhaustion)
● Administer
DIC
albumin, fresh
frozen plasma, Protracted
hetastratch, or vomiting,
dextran if diarrhea
cardiac output
still low
Nasogastric
suction
● Administer
isotonic
hypotonic
saline with
electrolytes as
needed to
maintain
normal
circulating
volume and
electrolyte
balance
SUMMARY OF THE MANAGEMENT OF
CARDIOGENIC SHOCK
Burns
Plasma loss
Etiology Clinical Intervention
Situation

Myocardia Acute M.I. ● Fluid challenge

l Disease with up to 300
or injury Myocardial mL of saline
contusion
solution or
Cardiomyopath lactated ringer’s
Accumulation solution to rule
ies
of intra- out
abdominal fluid hypovolemia,
unless heart
failure of
pulmonary
edema is
present.
Malnutrition ● Insert CVP or
pulmonary
artery catheter;
monitor cardiac
Severe
output,
dermatitis
pulmonary
artery pressure
and PCWP
DIC pressure, and
PCWP,
administer IV
fluids to
maintain left
ventricular
falling pressure
of 15-20 mmHg.
Dehydration ● Administer

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 SHOCK AND MULTISYSTEM DISORDERS
1.5 NCM 118: Critical Care Nursing
Dr. Socorro S. Gasco, RN, MN, DM • January 14, 2022

inotopics. External paracentesis.

(Dobutamine, Pressure Reduce
Pericardial
dopamine) on heart inspiratory
tamponade
vasodilators interferes pressure.
caused by
(Sodium with hear
trauma,
nitroprusside) interferen
aneurysm,
● Nitroglycerin, ces with
cardiac
Calcium channel heart
surgery, Treat
blockers filling or ●
pericarditis dysrhythmias;
(morphine) emptying
● Diuretics (eg: be prepared to
Mannitol or initiate CPR.
furosemide) Massive Cardiac pacing.
● Cadiotonics pulmonary
beta-blockers embolus
(eg:
Tension
propranolol)
pneumothorax
● Gluococorticoste
roids Intar- Ascites
aortic balloon
pump or Hemoperitoneu
external counter m
pulsation device Mechanical
if unresponsive Ventilation
to other
therapies

● Same as above:
if rapid response
does not occur,
prepare for
prompt cardiac
surgery

Cardiac
Dysrhyth Tachydysrythm
mia ias
● Relieve
tamponade with Bradydysrhyth
ECG assisted mias
pericardiocentes Pulseless
is; repair electrical
surgically if it activity
occurs.
● Thrombolytic
(streptokinase)
or anticoagulant
(heparin) SUMMARY OF THE MANAGEMENT OF
Valvular Ruptured aortic
therapy; surgical DISTRIBUTIVE SHOCK
Diseases cusp
or Injury for removal of
Etiology Clinical Interventions
Ruptured clot. Relieves air
Situation
papillary accumulation
muscle with needle Anaphylacti Allergy to food, ● Prepare for
thoracostomy or c shock medicines, surgical
Ball Thrombus
chest tube dyes, insect, management of
insertion. bites, stings, on airway.
● Relieve fluid latex Decrease
accumulation further
with

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 SHOCK AND MULTISYSTEM DISORDERS
1.5 NCM 118: Critical Care Nursing
Dr. Socorro S. Gasco, RN, MN, DM • January 14, 2022

absorption of cardiotonic
antigen (eg: agents
stop IV fluid, (dopamine or
place dobutamine,
tourniquet norepinephrine;
between isoproterenol,
injection or digitalis,
sting site and calcium
heart if feasible. ● Naloxone
Epinephrine (narcotic
1:100. antagonist)
● 2 inhalations ● Prostaglandins
every 3 hrs, or monoclonal
epinephrine antibodies
(1:1000) 0.2- Drotrecogin alfa
0.5 mL every 3- ● Temperature
15 minutes control (both
given hypothermia
Subcutaneously and
, or epinephrine hyperthermia
(1:10,000) 0.5- are noted)
1.0 mL every 5- ● Heparin,
15 minutes clotting factors,
given at a rate blood products
of 1 mg/min if DIC develops
● IV fluid ● Normal saline to
resuscitation restore volume
with isotonic
solution
Diphenhydrami
ne HCL or
● Theophylline IV ● Treat
drip from bradycardia
Septic Often gram-
bronchospasm with atropine
shock negative
Steroids IV ● Vasopressors
septicemia but
Vasopressors (norepinephrine
also caused by
(eg: , metaraminol
other organism
norepinephrine, bitartrate, high
in debilitated,
metaraminol dose dopamine,
immunodeficien
bitartrate. High and
t, or chronically
dose dopamine) phenylephrine)
ill clients
gastric lavage may be given.
for ingested ● Place client in
antigen ice pack modified
to injection or Trendelenburg
sting site position
● Meat tenderizer ● Place client in
paste to sing head down or
site recumbent
position

● Vigorous Iv fluid
resuscitation ● Give atropine if
with normal bradycardia and
saline profound
● Empirical hypotension
antibiotic ● Eliminate pain
therapy until
sensitivities are
reported
● Administer

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 SHOCK AND MULTISYSTEM DISORDERS
1.5 NCM 118: Critical Care Nursing
Dr. Socorro S. Gasco, RN, MN, DM • January 14, 2022

Severe pain

Severe
emotional
Vasovagal stress
reaction

3. Restore and maintain adequate perfusion

● Maintain an adequate circulating blood
volume
4. Nitric oxide
5. Vasoconstrictors
● They do favorably increase blood flow to
the brain and heart in severely
hypotensive clients
6. Vasodilators
● Include adrenergic blocking agents,
ganglionic blocking agents, and direct-
acting peripheral vasodilators.
● Adrenergic blockade prevents harmful
effects of prolonged vasoconstriction
such as increased pressure in capillaries,
promoting fluid loss from the vascular to
the interstitial compartment, and altered
blood flow, especially in the splanchic
area.
● Also used to keep the coronary arteries
open
● May be administered to inhibit
Spinal vasoconstriction of peripheral blood
anesthesia vessels (the result of norepinephrine
from sympathetic stimulation) so that
Spinal cord blood can be redistributed to enhance
injury tissue perfusion and increase vascular
volume
● Rapid and adequate fluid replacement
Neurogenic ● Keep clients who are receiving
(spinal) vasodilators lying relatively flat
Shock ● Elevation of the head can produce
dangerous orthostatic hypotension
7. Assist circulation
8. Intra-aortic balloon pump (IABP)
● Balloon-tipped catheter placed in the
descending thoracic aorta
● The catheter is attached to a unit that
inflate during diastole and deflates just
before the systole.
● Counter pulsation displaces blood back
into the aorta and improves coronary
artery circulation
● In cardiogenic shock, use of the IABP
reduces afterload, allowing the heart to
more efficiently empty, thereby,
increasing cardiac output.
9. Modified Trendelenburg position

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 SHOCK AND MULTISYSTEM DISORDERS
1.5 NCM 118: Critical Care Nursing
Dr. Socorro S. Gasco, RN, MN, DM • January 14, 2022
● Lower extremities elevated 30-45
degrees
● Knees straight, trunk horizontal or very
slightly raised and the neck comfortably
positioned with the head level with the
chest or slightly higher.
● The traditional Trendelenburg position
(head down, with legs elevated at least
30 degrees above the head), was once
the classic shock position but is no longer
used for shock management because it
compresses the abdominal contents
against the diaphragm, interfering with
pulmonary excursuion
● And promotes congestion of blood in the,
possibly contributing to cerebral
10. Replace fluid volume
● Aggressive fluid replacement should be
tapered off when urine output is at least
0.5 mL/kg/hr, systolic BP is greater than
100 mmHg, or the heart rate is 60 to 100
bpm
11. Blood
● Rapid administration of large volumes of
packed cells or whole blood may be
necessary
● Crystalloid is usually given as an initial
emergency treatment to sustain BP.
12. Autotransfusion
● Involves collecting and retransfusing
blood into the same client
● Used to prevent or treat hypovolemic
shock cause by hemorrhage
13. Crystalloid or balanced salt solutions
● Warmed crystalloids or balance salt
solutions, colloids, and blood
● Dextrose and water should not be used
to resuscitate a client; once the dextrose
is metabolized, only hypotonic water
remains, which leads to greater fluid
shifts. Electrolyte solutions such as
ringer’s lactate help expand extracellular
volume reduce viscosity and prevent
sludging. In a client with impaired liver
function, a solution containing lactate
could further compound the problem of
lactic acidosis
● Lactate is converted to bicarbonate and
does not accumulate
14. Colloid solution
● Most commonly used colloid solutions
include plasma and its components,
plasma substitutes (dextran), oxygen-
carrying solutions other than blood (eg:
perfluorocarbons and ultra-purified,
stroma-free hemoglobin solution), and
hetastarch
● Fresh frozen plasma (FFP) is the form
commonly used to improve serum
protein levels
15. Blood substitutes
● Perfluorocarbon (eg: fluosol, oxygen) are
non-blood, oxygen-carrying solutions
that remain in the circulation for about
12-24 hours
● Hetastarch, a glycogen-like synthetic
BAUTISTA, BALMES, BELARMINO, BARCELON
colloid has been used to treat
hypovolemic shock and may provide
alternatives to blood administration. Its
effect last between 3 and 24 hours.
● Pentastarch is also available as volume
expander
16. Evaluate fluid replacement
17. Prevent renal impairment
18. Prevent gastrointestinal bleeding
19. Provide pharmacologic management
● Antibiotic (ex: gentamicin, amikacin) are
common first line choice for antibiotic
therapy
● Drotrecogin alfa
▪ Drotrecogin alfa (xigris) I used
for severe sepsis and SIRS.
Drotrecogin alfa is recombinant
form of human activated protein
C and has the ability to inhibit
inflammation, inhibit
coagulation, and promote
fibrinolysis. The main effect of
protein C is to reduce the
production of thrombin by
inactivating factors Va and VII
● Heparin
▪ The anticoagulant effect of
heparin may help prevent
complications or treat DIC
▪ The treatment if DIC may include
heparin administration to
minimize consumption of clotting
factors.
● Steroids
▪ Are given to reduce edema in the
cord and have been shown to
improve recovery. They assist in
treatment by stabilizing
lysosomal membrane and
preventing intracellular release
of enzymes
● Naloxone
▪ Used to treat opioid and
synthetic opioid over dosages
▪ During stress, opioid like
substances known as
enkephalins and endorphins are
released from the brain
▪ May play a role in capillary bed
vasodilation found in all forms of
shock
● Insulin
● Epinephrine
▪ Drug choice for treatment of
allergic reaction
▪ Inhibits histamine release and
antagonizes its effects on end
organs, resulting in reversal of
the bronchial constriction,
increased capillary permeability
and vasodilation that occur with
acute anaphylactic reactions.
● Proton pump inhibitors, Sucralfate, and
Histamine H2-Receptor Antagonists
▪ Inhibits gastric acid secretion
▪ Stress ulcers are often lethal
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 SHOCK AND MULTISYSTEM DISORDERS
1.5 NCM 118: Critical Care Nursing
Dr. Socorro S. Gasco, RN, MN, DM • January 14, 2022
complications of severe illness or
injury produced by continuous
shunting of blood from the GI
tract due to extended
sympathetic nervous system
stimulation.
● Opioids
● Cardiotonic Medications
▪ Beta blockers and calcium
channel blockers
▪ Amiodarone, lidocaine,
bretylium, quinidine,
procainamide may treat
dysrhythmias that tend to reduce
cardiac efficiency
● Calcium
NURSING MANAGEMENT OF THE MEDICAL
CLIENTS
1. Oxygenation monitoring
2. Perfusion monitoring
→ Assess the client’s pulse, BP, skin,
temperature, heart sounds, peripheral
pulses, state of hydration, and skin
perfusion (ex: capillary refill time less
than 3 seconds)
3. BP monitoring
4. Temperature monitoring
5. Cardiac monitoring
→ ECG monitor
→ CVP line placement
6. Hemodynamic monitoring
→ Measurement of CVP
→ Pulmonary artery and pulmonary
capillary wedge pressure (PCWP)
→ Measurement are monitored to assess
left-sided heart function and to guide
fluid administration.
7. Cardiac output monitoring
→ Swan-Ganz catheters and the ease of
obtaining measurements.
8. Prevent complications
→ Additional assessments important in
preventing complications include
evaluation of the following :
- Level of consciousness and orientation
- Ability to move extremities
- Sensation in all extremities
- Hand grasps
- Response to verbal and painful stimuli
- Pupil size and reaction to light
- Bowel sounds
- Abdominal distention
- Bone deformities
9. Prevent renal impairment
→ Indwelling catheter
→ Assess the client’s urine output routinely
and recore it at least every hour.
10. Prevent gastric ulceration
● Guaiac solution can be used to check for
blood; litmus paper checks the pH to
determine the acidity of the stomach.
BAUTISTA, BALMES, BELARMINO, BARCELON
DIAGNOSIS
● Ineffective tissue perfusion
● Interrupted family processes
● Activity intolerance
● Acute pain
● Anticipatory grieving
● Anxiety
● Bathing/hygiene, dressing/grooming,
toileting, self-care deficit
● Compromised family coping
● Constipation
and ● Decreased cardiac output
● Deficient fluid volume
● Disturbed body image
● Disturbed personal identity
● Disturbed sleeping pattern
● Disturbed sensory perception: visual
auditory, kinesthetic, gustatory, tactile,
olfactory.
● Fear
● Imbalanced nutrition: less than body
requirements
● Impaired gas exchange
● Impaired physical mobility
● Impaired or risk for impaired skin integrity
● Impaired verbal communication
● Ineffective airway clearance
● Ineffective breathing pattern
● Ineffective protection
● Ineffective tissue perfusion: cerebral,
cardiopulmonary, gastrointestinal, renal,
peripheral
● Interrupted family processes
● Spiritual distress
MULTIPLE ORGAN DYSFUNCTION
SYNDROME
● Multiple Organ Dysfunction Syndrome (MODS),
Multiple Organ System Failure, r Multi-organ
system failure
→ Is considered to be present when two
or more organs fail
ETIOLOGY AND RISK FACTORS
→ Dead tissue
→ Injured tissue
→ Infection
→ Perfusion deficit
→ Persistent sources of inflammation such
as pancreatitis or pneumonitis.
→ Acute lung injury
● People known to be at high risk*
- Older adults
- Clients with chronic illnesses
- Clients with malnutrition
- Clients with cancer
- Prolonged or exaggerated inflammatory
responses
- Victims of severe trauma
- Clients with sepsis
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 SHOCK AND MULTISYSTEM DISORDERS
1.5 NCM 118: Critical Care Nursing
Dr. Socorro S. Gasco, RN, MN, DM • January 14, 2022

PATHOPHYSIOLOGY: → Body engages in auto catabolism, which

→ Integrated inflammatory immune response (IIR) causes profound changes in the body’s
protects tissue from microbial invasion and rids metabolic processes
the body of cellular debris and foreign material’ → Outcome for the client is death.
→ Bacteria introduced into the wound or allowed
to grow in necrotic tissue because of a CLINICAL MANIFESTATION
decreased immune response activate the → Aspiration
systemic inflammatory responses → Ruptured aneurysm
→ Bacteria release txins that activate systemic → Septic shock
medications of inflammation → Hypotension
→ Once the inflammatory response becomes → Low grade fever
systemic, it is controlled by chemical mediators → Tachycardia
of inflammation. → Increased numbers of banded and
→ Mediators include bradykinin complement, Segmented Neutrophils
histamine, interleukin-1, prekallikrein, → Dyspnea – Intubation And
prostaglandins and tumor necrosis factor (TNF) Mechanical Ventilation Are
→ These powerful mediators of inflammations Required
induce a systemic response. → DIC Is Usually Present
→ The endothelium is destroyed and blood flow is → Increased Cardiac Index (Greater
reduced to the tissues Than 4.5 L/Min)
→ Endothelial damage is produced by endotoxins → Systemic Vascular Resistance Of Less
from bacteria, tumor necrosis factor, Than 600 Dynes Cm-5
interleukin-1, platelet activating factors and → Increased Blood Glucose
many others → Bilirubin Level Increases
→ It produces damage to organs and tissues by → Increase In Serum Creatinine
altering perfusion, disturbing oxygen supply or → Blood Glucose And Lactate Levels
demand or hanging metabolic dysfunctions Continue To Increase Because Of
→ Metabolism increases under the direction of The Hypermetabolic State
mediators such as cortisol and the → Excretion Of Urinary Nitrogen And
catecholamines Protein
→ The lungs are usually the first to malfunction, → Decreased Levels Of Serum Albumin,
because of the large surface area of pulmonary Pre-Albumin And Retinol
epithelium combined with the presence of → Candida And Viruses
bacterial contamination from systemic blood → Cytomegalovirus
return → Surgical Wounds To Fail To Heal
→ The GI tract is general the second system to → Pressure Ulcers May Develop
malfunction, and it propagates conditions for → Renal Failure Worsens
further deteriorations of other organs. → Edema May Be Present Because Of
→ The hypermetabolic state increases gastric acid Low Serum Protein Levels
production, increasing the risk of ulceration and → Lactic Acidosis Worsens, Liver
bleeding. Enzymes Continue To Increase.

CLASSIFICATION: MEDICAL MANAGEMENT

1. Primary MODS
→ Results directly from “a well-defined
insult in which organ dysfunction occurs
early and is directly attributed to the
insult itself.
→ The direct insult initially causes to
localized inflammatory response that
may or may not progress to SIRS.
2. Secondary MODS
→ Is a consequence of widespread
systemic inflammation, which develops
after a variety of insults and results in
dysfunction of organs not involved in the
initial insult
1. Restrain The Activators
→ Antibiotics
→ Large Infected Wound Incised And
Drained Or Necrotic Tissue Excised
→ Nutrient Intake Is Usually 30 To 35
Kcal/Kg/Day Of Carbohydrates
→ Proteins Are Given To The Client Via
Modified Amino Acids
2. Control The Mediators
→ Maintenance of A Positive Nitrogen
Balance Via Nutrition, Promotion Of
Sleep And Rest And Management Of
Pain.
→ Monoclonal Antibodies To Control
Mediators Such As Interleukin-1,
Endotoxins And Tumor Necrosis Factor

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 SHOCK AND MULTISYSTEM DISORDERS
1.5 NCM 118: Critical Care Nursing
Dr. Socorro S. Gasco, RN, MN, DM • January 14, 2022

3. Protect The Affected Organs Treatment of infection ● Monoclonal

→ Client Is Intubated An Mechanically antibodies
Ventilated To Maintain Adequate ● Positive antibody
Oxygenation protection
→ Fluids And Inotropic Drugs Are Used To ● Gut
Support Hemodynamic Parameters
decontamination
→ Nutritional Supports Also Critical To
regimens
Reduce the Catabolism That
Accompanies Hyper Metabolism. Support of Gut functions ● Mucosal trophic
Dialysis Is Often Used To Reduce agents:
Azotemia From Renal Failure.
e.g glutamine,
Modified Apache II Criteria for Diagnosis of Multiple bombesin, ketone
Organ Dysfunction Syndrome bodies

● Cardiovascular Failure (Presence of One or More ● Early enteral

of the Following) feeding
→ Heart rate <54 beats/min ● Regulation of gut
→ Mean arterial pressure ≤ 49 mmHg (systolic microbial flora
pressure ≤ 60 mmHg)
→ Occurrence of ventricular tachycardia or Improved resuscitation ● Hypertonic saline
ventricular fibrillation ● In-line sensors
→ Serum pH ≤7.24 with a PaCO2 of ≤40 mmHg ● Tissue-specific
sensors
● Respiratory Failure (Presence of One or More of ● Noninvasive
the Following) monitoring
→ Respiratory rate ≤5 breaths/min or ≤49
breaths/min PaCO2 ≥ mmHg Endothelial cell ● PAF inhibitors
→ Alveolar – arterial oxygen difference ≥350 mmHg protection ● WBC adherence
(calculate as follows, at sea level (713 x % oxygen inhibition
in inspired gas) – PaCO2 – PaO2 ) ● Antioxidant
→ Dependent on ventilator or CPAP on the second therapy
day ● Eicosanoid
modulation
● Renal Failure (Presence of One or More of the
Following) Modulation of ● N3
→ Urine output ≤479 ml/24 hr or ≤1.59 ml/8 hr macrophage function polyunsaturated
→ Serum BUN ≥100 mg/dl (35.7 mmol/L) fatty acids
→ Serum creatinine ≥3.5 mg/dl (309 umol/L) ● Signal
● Hematologic Failure (Presence of One or More of transduction
the following)
modulation
→ WBC count ≤1000/µl (1 x 10^9/L)
→ Platelets ≤20,000/µl (20 x 10^9/L) Stimulation of ● Arginine
→ Hematocrit ≤20% lymphocyte function ● W3
polyunsaturated
● Neurologic Failure fatty acids
→ Glasgow Coma Scale score ≤ 6 ( in absence of
sedation )

● Hepatic Failure (Presence of Both the Following) ⎯

→ Serum bilirubin ≥6 mg%
→ Prothrombin time ≥4 sec over control in the
absence of systemic anticoagulation

Summary of Potentially Useful Therapies for multiple

Organ Dysfunction Syndrome

Rationale Therapy

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